异氟醚对幼年大鼠认知损伤的机制及研究进展  

Mechanism and research advances of isoflurane on cognitive impairment in young rats

作　　者：王雪 刘洪涛[1] 

机构地区：[1]中国医科大学附属盛京医院麻醉科,沈阳110004

出　　处：《国际麻醉学与复苏杂志》2017年第11期1054-1056,I0001,共4页International Journal of Anesthesiology and Resuscitation

基　　金：国家自然科学基金（81271370）

摘　　要：背景异氟醚作为儿科和产科手术过程中常用的吸入性麻醉药，因其麻醉深度易掌控、对循环影响小等优点，被广泛应用于临床。目的近年来有报道称幼年时期反复多次或长时间暴露于麻醉药物会引发远期记忆缺失。因此，异氟醚的神经损伤作用机制受到广泛关注。内容总结近5年异氟醚毒性机制研究，概括为：损伤突触可塑性产生神经毒性、抑制N－甲基－D－天门冬氨酸（N-methyl-D-aspartate，NMDA）受体并且兴奋γ-氨基丁酸A型受体（gammaamino acid type Areceptor，GABAAR）影响长时程增强的产生、干扰钙稳态、激发神经营养因子产生凋亡通路认知以及其他可能的毒性机制。趋向进一步明确研究方向，为将基础研究已取得的成果转化到临床实践、为新药和保护药物的研发提供参考依据。Background Isoflurane is an inhaled anesthetic widely used in pediatric and obstetric operations, due to its advantages such as anesthesia depth which is easy to control and little influence on the circulation. Objective Recent reports showed that repeated or long-time exposure to anesthetics at the young stage may cause deficient memory in the future. Therefore, increasing attentions have been drawn on isoflurane＇s mechanism about neurological damages. Content This paper summarized the toxic mechanism of isoflurane in the recent five years, and synaptic plasticity damages can cause neurotoxicity, inhibit N-methyl-D- aspartate （NMDA） receptor and stimulate amino acid type A receptor （GABAAR） and affect long-term potentiation, calcium homeostasis, and activate neurotrophins to produce apoptotic pathway, and other possible toxic mechanisms. Trend This paper can further determine the research direction, providing references for transform of basic research data into clinical practice as well as for the research and development of new protective drugs.

关 键 词：异氟醚 发育期大脑 凋亡 神经毒性 突触 

分 类 号：R614[医药卫生—麻醉学]